ChAT Expression in Chlamydia muridarum-infected Female Murine Genital Tract

Chlamydia trachomatis is the most prevalent agent of bacterial sexually transmitted infections in the world. However, a profuse number of cases are unreported, as the infection is often asymptomatic. Sequelae such as pelvic inflammatory disease, an increased risk of cervical cancer, premature birth, and perinatal infections in pregnant women can occur. Inflammation occurs in the body in response to infection or injury. Although inflammation can lead to some unwanted secondary effects, such as pain, it serves to return the body to homeostasis by restoring injured tissues and eliminating pathogens. One recently identified connection between the central nervous system and the immune system that regulates inflammation is the cholinergic anti-inflammatory pathway (CAP). In the CAP, pathogen-associated molecular patterns stimulate the vagus nerve to activate the pathway, which ultimately results in acetylcholine (ACh) release, which down regulates inflammation. We hypothesized that genital chlamydial infection would increase the expression of choline acetyltransferase (ChAT), the enzyme that synthesizes ACh, in the female murine genital tract, therefore down regulating inflammation and promoting chlamydial infection. Transgenic female mice carrying a ChAT-promoter driven GFP reporter gene were vaginally infected with C. muridarum. Mice were sacrificed on days 3, 9, 15, and 21 post infection; cervical, uterine horn, and ovarian tissues were removed and embedded in paraffin. Small sections of each tissue were cut and mounted onto slides. The tissue sections were then stained for the expression of ChAT using immunohistochemical techniques. Finally, tissue sections were viewed under a microscope for positive staining and the data was analyzed. The results indicated that there is a significant increase in the number of cells that express ChAT in genital tract of chlamydia-infected mice versus non-infected mice